I hope I never need to know this but why are statins bad? What is their purpose and what effect did they have on you?
I hope I never need to know this but why are statins bad? What is their purpose and what effect did they have on you?
Before my father had his heart attack (late 1970s), his triglycerides were over 400 which is very high. He ate plenty of white carbs, yet he wasn’t overweight. He switched to whole grain, fruits and vegs (fibrous carbs) and his trigs dropped to low 100 range.
They’ve actually been proven to cause diabetes. They made my glucose and a1c ( i think that was it, the other measure of sugars) skyrocket. They gave me a very uneasy, off feeling. There’s alot more negatives, too many to go into detail(research). When there is 0 copay for a medication through insurance, there’s a reason for that! I’ve tried them for 2 different runs in past 6-7 yrs, both with negative effects
Yes, there are exceptions to the secondary preventive rule (cardiovascular events) where statins are recommended - namely hereditary hyperlipidemias which can be seen in 1/200-300 people, and diabetes (which in itself increases the cardiovascular risk).
Statins for people with a low risk of cardiovascular disease show no significant mortality benefit. According to NNT (numbers needed to treat), one out of 217 treated people avoid a nonfatal myocardial infarction, one of 313 avoided a nonfatal stroke. As for harms, one out of 21 (!) experience pain (from muscle damage). I think these numbers may have changed lately, but the conclusion remains the same.
Re @melisnmatt comment, one out of 204 people develop diabetes. If you were to take statins for 5 years, one out of 50 people will develop diabetes.
Furthermore, the SCORE algorithm to estimate cardiovascular risk has it’s pros and cons, but can be used to discuss and motivate changes in lifestyle with the individual patient.
There is good science showing the link between statins and poor blood sugar control. Heck, even some of the drug manufacturers acknowledge this on their labelling. The FDA issued this drug safety notice several years ago: ‘FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs’. It states:
Increases in glycosylated hemoglobin (HbA1c) and fasting plasma glucose
FDA’s review of the results from the Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) reported a 27% increase in investigator-reported diabetes mellitus in rosuvastatin-treated patients compared to placebo-treated patients.
There has been a greater risk reported elsewhere. For example, a review was conducted using data from the famous $700m ‘Women’s Health Initiative’ study (see ‘Statin Use and Risk of Diabetes Mellitus in Postmenopausal Women in the Women’s Health Initiative’). It found subjects on statins had a 48% increased risk of diabetes.
Hopefully, no one is intentionally prescribing statins for people at low risk. Now that raises the question of whether or not one can correctly identify people who are at high risk.
I get that over-reliance on cholesterol tests, particularly a single measure like total or LDL, may lead to over-prescribing statins. I also understand that some people with “OK” or even “good” cholesterol numbers can have heart attacks. But I’m not sure that means someone with a poor lipid profile, elevated blood sugar, and other symptoms of metabolic syndrome should say that the cholesterol hypothesis is bogus, therefore I’m not going to worry about it. After all, heart disease (which covers a lot of different medical conditions) is still the leading cause of death in the US.
My frustration is this: if you have some red flags (lipids, blood sugar, blood pressure, struggles with weight), what should you do? Lifestyle modifications are of course advisable. Change diet? Sure, but to what: Mediterranean, extreme low fat (ala Ornish and Esselstyn), extreme low carb (Volek, Ivar Cumming, et al.)? They all make persuasive cases. Who is right? Who has the best evidence in support of their favored dietary intervention?
And some of us continue to have some of these red flags, even after losing weight, trying various diets, exercising regularly. Should you assume you are good, and then wait and see if you have a heart attack. Then if you have one and survive, consider a statin? Or maybe get a Coronary Artery Calcium Scan? (What is the thinking in your country about those?)
Doing your own research can be exhausting, and you can end up running down a lot of rabbit holes.
One of the issues is that some people, and I include so-called ‘authorities’ on the subject, refuse to recognise science when it is in front of their faces.
You have cited a classic example - diets. Who is right? Well, I can tell you what the science says: between 2003-2018, there were 62 randomised controlled trials comparing low fat diets to lower carb diets (i.e. less than 130g) for weight loss. Of these, 31 provided statistically significant findings (i.e. unlikely to be random chance). In every single one, the group on the lower carb diet had the greatest weight loss. Now I can hear the naysayers grumble but that is the data.
Here are the 5 key markers everyone should keep an eye on:
The definition, metabolic syndrome is present if three or more of the following five criteria are met: waist circumference over 40 inches (men) or 35 inches (women), blood pressure over 130/85 mmHg, fasting triglyceride (TG) level over 150 mg/dl, fasting high-density lipoprotein (HDL) cholesterol level less than 40 mg/dl (men) or 50 mg/dl (women) and fasting blood sugar over 100 mg/dl.
I was thinking specifically about mortality and cardiovascular disease, not weight loss.
I’ve tried low carb diets, and had some success with (spontaneous) weight loss. But it didn’t get me to my weight target. I stalled, and found myself dealing with hunger issues, despite the lack of carbs in the diet. I also found that after an initial drop in A1C, my blood sugar levels rebounded once I was weight stable on the low carb diet. I even doubled down, and tried the nutritional ketosis thing for awhile. I remember that I felt like crap.
Well they are not mutually exclusive!
Of course, we are all prone to judge from our own personal experience. I have had the polar opposite experience on low carb (keto) both in terms of how I felt and by measurable results (fat/lean tissue mass, various blood work, ketone and blood glucose levels).
A fellow at work has been a college level swimmer for over 30 years . He can easily swim 5 miles and has an incredibly slow heart beat and is in great condition. A few years ago while swimming a chunk of plaque dislodged from a artery or vein and blocked his heart and it almost killed him. They called it the widow maker. He got some stints and they put him on some statins. He was back to work and swimming in no time. I think he has genetically high cholesterol? He stopped eating all junk and went on a diet he called sticks and grass and with that and the statins his cholesterol went way down. A few years into the diet he had to stop the statins for a short while and while still on the sticks and grass diet his cholesterol shot back up. It seems his diet didn’t phase his cholesterol.
HDL/LDL ratio should be in there.
People with high LDL almost always see it drop when they improve their lifestyle (lose weight, etc.), get more fit, improving what they eat, etc.
C–Reactive Protein which measures inflammation is another important data point. Homocysteine another.
This is a poorly understood topic. LDL has earned the tag ‘bad cholesterol’ on completely bad science. High LDL is not by itself a problem. I won’t rehash this again but I will pose a question:
If raised LDL is a bad sign, why does prolonged bouts of fasting raise LDL? After all, by consuming nothing surely my lipids wouldn’t get ‘worse’?
Problems with studies,
Low fat diets used in these studies are not usually 10 % or less of macronutrients.
The same is true of low carb diet studies.
You can not always trust studies on these issues.
I believe both diet types can be useful at times.
For example, glycogen replenishment post workout.
If you consume nothing, then would die. So, surely you’re eating ‘something’ while fasting. There needs to be context around this. What is being consumed and how much in conjunction to activity levels, etc. could dictate LDL. For example, If one is eating a 2000 calorie meal once a day full of higher saturated fat, processed cooked oils, etc., and non-active versus three meals at 2000 calories day and full of high monosaturated fats instead, all things being equal, the 2000 calorie higher saturated fat once a day meal will likely increase LDL before the 2000 calories high mono-fat a day/split over 3 meals who is active, exercises, etc.
I would like to see peer-reviewed studies showing how fasting in and of itself causes increased LDL. You are the very first person I’ve read stating such as fact.
You are raising some serious questions here. One pragmatic way of dealing with risk factors is to prioritize (and perhaps change one thing at a time, for evaluation). Smoking is obviously the number one risk factor to eliminate. There should be no misconception re high blood pressure being more important to control than lipids. The blood pressure rises along with age, and excercise have surprisingly little effect upon it from a population based perspective (not neglecting greater individual responses). Excercise in itself has benefits in every aspect, but I will not channel in on it here.
Re diets as a lipid lowering strategy, I prefer to recommend simple changes that will be manageble over time, to the individuals diet. No excesses or extremes in terms of specific diets, as I tend to respect the current “Nordic” dietary recommendations (not much different from the US recommendations). Once again, I have seen patients who have gone their own route (most commonly chosen the no-carb way) with good results - But, these people are few. This tells me though, that it may be necessary to put an individual perspective on diets - if the regular recommendations does not provide any result. A consultation with an open minded dietician can here be recommended.
As for continued “red flags” even though having tried various strategies - I would follow these patients regularly, to make sure the parameters and labs are steady.
As a sidenote I have recently noticed subjective stress and sleep disorders as problematic areas in respect of the above discussion.
The Coronary Artery Calcium Scan is a very interesting one. I’ve read pros and cons on it.
What? People can do water-only fasts for days on end, even a week at a time. Fasting means fasting.
If you are fasting, you are not consuming externally provided energy. But you are using up internal stores of energy. So, in some sense, the body basically starts eating itself. You pull glucose out of glycogen, and fats out of adipose tissue. Once your glycogen stores get depleted, the body will make whatever glucose it needs by breaking down protein. The majority of energy will come from adipose tissue. So perhaps fasting ends up being something like eating a high fat diet, with the composition of the fats being determined by what sorts of fats you’ve stored in your body?
Really? This is not new. In fact, data collected from tertiary outcomes of the 2010 FEELGOOD Trial, which examined the effect of fasting on physical changes related to cardiovascular disease, was presented at a meeting of the American College of Cardiology back in 2011. In short, it stated: 'A 24-hour fast consisting only of water causes an acute increase in total serum cholesterol by raising both LDL cholesterol and HDL cholesterol…’
This makes perfect sense, i.e. the increased free fatty acid turnover from fasting necessitates a greater number of LDL particles to accommodate the energy shift. That’s what LDL does. It ferries cholesterol to every cell in the body.